The aim of this study is to continue to investigate the role of circulating triglyceride-fatty acids in lung metabolism and surfactant synthesis. Triglycerides do not penetrate the endothelial barrier. Chylomicron and very low density lipoprotein bound triglycerides are first hydrolyzed by lipoprotein lipase (LPL) on or near the endothelial surface. We have established that triglyceride-fatty acids are precursors of lung phospholipid and that endothelial integrity, i.e. LPL activity are essential for their incorporation. We shall now study: (1) The role of LPL in delivery of circulating lecithin and lysolecithin to the lung in the adult and fetal rat. (2) The mechanism of action and the mode of endothelial transport of LPL. (3) The age dependence and significance of lung LPL in the production of lipoprotein-remnants. The following hypotheses remain to be tested: (1) LPL activity is a sensitive indicator of endothelial function in the lung. (2) Lung endothelium might selectively affect lipoprotein remnants and very low density lipoproteins and therefore modify the level of atherogenic substances in the systemic circulation.